Article Dans Une Revue Proceedings of the National Academy of Sciences of the United States of America Année : 2018

TP53INP1 deficiency maintains murine B lymphopoiesis in aged bone marrow through redox-controlled IL-7R/STAT5 signaling

Résumé

Significance Reactive oxygen species (ROS) play a role in signaling in immune cells, in particular in B cell activation and terminal differentiation in secondary lymphoid organs. Nevertheless, their role in B cell development in the bone marrow (BM) still remains poorly explored. TP53INP1 is a target of the tumor suppressor p53, which mediates its antioxidant activity. We report the surprising observation that chronic oxidative stress in TP53INP1-deficient mice rescues B lymphopoiesis in the BM during aging. ROS sustain IL-7R signaling in aged TP53INP1-deficient BM through maintenance of active STAT5 transcription factor, driving the expression of the B lineage Pax5 transcription factor. This work suggests that antioxidants cannot be in favor of antibody-producing cell development.

Dates et versions

hal-04772663 , version 1 (08-11-2024)

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Bochra Zidi, Christelle Vincent-Fabert, Laurent Pouyet, Marion Seillier, Amelle Vandevelde, et al.. TP53INP1 deficiency maintains murine B lymphopoiesis in aged bone marrow through redox-controlled IL-7R/STAT5 signaling. Proceedings of the National Academy of Sciences of the United States of America, 2018, 116 (1), pp.211-216. ⟨10.1073/pnas.1809980116⟩. ⟨hal-04772663⟩
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